Past events

For centuries, consciousness was considered to be outside the reach of scientific investigation. Yet in recent decades, more and more studies have tried to probe the neural correlates of conscious experience, and several neuronally-inspired theories for consciousness have emerged. In this talk, I will focus on four leading theories of consciousness: Global Neuronal Workspace (GNW), integrated Information Theory (IIT), Recurrent Processing Theory (RPT) and Higher Order Theory (HOT). I will first shortly present the guiding principles of these theories. Then, I will provide a bird's-eye view of the field, using the results of a large-scale quantitative and analytic review we conducted, examining all studies that either empirically tested these theories or interpreted their findings with respect to at least one of them. Finally, I will describe the first results of the Cogitate consortium - an adversarial collaboration aimed at testing GNW and IIT.

How information is processed within the brain is a key question in systems neuroscience. We address the issue in spiking neuronal networks of freely moving mice. I will describe our recent findings and conclusions pertaining to three specific information processing steps: transmission, representation, and storage. First, using feedforward optogenetic injection of white noise input to a small group of adjacent neocortical excitatory cells, we find that spike transmission to a postsynaptic cell exhibits error correction, improved precision, and temporal coding. The results are consistent with a nonlinear coincidence detection model in the postsynaptic neuron. Second, by triggering input on animal kinematics, we create an artificial place field in an otherwise-silent pyramidal cell. In hippocampal region CA1 but not in the neocortex, artificial fields exhibit synthetic phase precession that persists for a full cycle. The local conversion of an induced rate code into an emerging phase code is compatible with a dual-oscillator interference model. Third, by triggering input on spontaneous spiking, we impose self-terminating spike patterns in a group of presynaptic excitatory neurons and a postsynaptic cell. The precise timing of all pre- and postsynaptic spikes has a more substantial impact on long-lasting effective connectivity than that of individual cell pairs, revealing an unexpected plasticity mechanism. We conclude that intrinsic properties of single neurons support millisecond-timescale operations, and that cortical networks are organized in functional modules which we refer to as “converging assemblies”.

In families with febrile seizures and temporal lobe epilepsy, mutations affecting different GABAergic mechanisms suggest that failure of chloride conductance to limit depolarization may be directly epileptogenic. This “GABAergic disinhibition” hypothesis has been discounted historically for two reasons. First, early attempts to produce hippocampal sclerosis and epilepsy simply by eliminating hippocampal GABA neurons consistently failed to do so. Second, the notion persists that because clinical epilepsy diagnosis is typically delayed for years or decades after brain injury, temporal lobe epileptogenesis should be presumed to involve a complex pathological transformation process that reaches completion during this “latent period.” Recent advances clarify both issues. Although spatially limited hippocampal GABA neuron ablation causes only submaximal granule cell hyperexcitability, more spatially extensive ablation maximizes granule cell hyperexcitability and triggers nonconvulsive granule cell status epilepticus, hippocampal sclerosis, and epilepsy. Recent studies also show that disinhibited granule cells begin to generate clinically subtle seizures immediately post-injury, and these seizures then gradually increase in duration to become clinically obvious. Therefore, rather than being a seizure-free “gestational” state of potentially interruptible epileptogenesis, the “latent period” is more likely an active epileptic state when barriers to seizure spread and clinical expression are gradually overcome by a kindling process. The likelihood that an epileptic brain state exists long before clinical diagnosis has significant implications for anti-epileptogenesis studies. The location, magnitude, and spatial extent of inherited, autoimmune, and injury-induced disinhibition may determine the latency to clinical diagnosis and establish the continuum between the benign, treatable, and refractory forms of temporal lobe epilepsy.

For centuries, consciousness was considered to be outside the reach of scientific investigation. Yet in recent decades, more and more studies have tried to probe the neural correlates of conscious experience, and several neuronally-inspired theories for consciousness have emerged. In this talk, I will focus on four leading theories of consciousness: Global Neuronal Workspace (GNW), integrated Information Theory (IIT), Recurrent Processing Theory (RPT) and Higher Order Theory (HOT). I will first shortly present the guiding principles of these theories. Then, I will provide a bird's-eye view of the field, using the results of a large-scale quantitative and analytic review we conducted, examining all studies that either empirically tested these theories or interpreted their findings with respect to at least one of them. Finally, I will describe the first results of the Cogitate consortium - an adversarial collaboration aimed at testing GNW and IIT.

How information is processed within the brain is a key question in systems neuroscience. We address the issue in spiking neuronal networks of freely moving mice. I will describe our recent findings and conclusions pertaining to three specific information processing steps: transmission, representation, and storage. First, using feedforward optogenetic injection of white noise input to a small group of adjacent neocortical excitatory cells, we find that spike transmission to a postsynaptic cell exhibits error correction, improved precision, and temporal coding. The results are consistent with a nonlinear coincidence detection model in the postsynaptic neuron. Second, by triggering input on animal kinematics, we create an artificial place field in an otherwise-silent pyramidal cell. In hippocampal region CA1 but not in the neocortex, artificial fields exhibit synthetic phase precession that persists for a full cycle. The local conversion of an induced rate code into an emerging phase code is compatible with a dual-oscillator interference model. Third, by triggering input on spontaneous spiking, we impose self-terminating spike patterns in a group of presynaptic excitatory neurons and a postsynaptic cell. The precise timing of all pre- and postsynaptic spikes has a more substantial impact on long-lasting effective connectivity than that of individual cell pairs, revealing an unexpected plasticity mechanism. We conclude that intrinsic properties of single neurons support millisecond-timescale operations, and that cortical networks are organized in functional modules which we refer to as “converging assemblies”.

In families with febrile seizures and temporal lobe epilepsy, mutations affecting different GABAergic mechanisms suggest that failure of chloride conductance to limit depolarization may be directly epileptogenic. This “GABAergic disinhibition” hypothesis has been discounted historically for two reasons. First, early attempts to produce hippocampal sclerosis and epilepsy simply by eliminating hippocampal GABA neurons consistently failed to do so. Second, the notion persists that because clinical epilepsy diagnosis is typically delayed for years or decades after brain injury, temporal lobe epileptogenesis should be presumed to involve a complex pathological transformation process that reaches completion during this “latent period.” Recent advances clarify both issues. Although spatially limited hippocampal GABA neuron ablation causes only submaximal granule cell hyperexcitability, more spatially extensive ablation maximizes granule cell hyperexcitability and triggers nonconvulsive granule cell status epilepticus, hippocampal sclerosis, and epilepsy. Recent studies also show that disinhibited granule cells begin to generate clinically subtle seizures immediately post-injury, and these seizures then gradually increase in duration to become clinically obvious. Therefore, rather than being a seizure-free “gestational” state of potentially interruptible epileptogenesis, the “latent period” is more likely an active epileptic state when barriers to seizure spread and clinical expression are gradually overcome by a kindling process. The likelihood that an epileptic brain state exists long before clinical diagnosis has significant implications for anti-epileptogenesis studies. The location, magnitude, and spatial extent of inherited, autoimmune, and injury-induced disinhibition may determine the latency to clinical diagnosis and establish the continuum between the benign, treatable, and refractory forms of temporal lobe epilepsy.